OSCR

The therapeutic effect and specific mechanism involved active Chinese medicine component biochaninA in glioma.

Overview

Authors: Dan Chai1, Mengran Xi2, Lu Gao3, Lei Sun4, Desong Kong1, Yujie Zhu1, Jinghua Zhang1, Qiang Cai3, Xinru Xiao5, Changqing Wang6
  1. Nanjing Hospital of Chinese Medicine Affiliated to Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China
  2. Fudan University – Dr. Kong Joint Research Center for Sports Medicine and Health Footwear, Fudan University Institute of Sports Medicine (Jinqiao Laboratory), Shanghai, China
  3. Department of Neurosurgery, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China
  4. Acupuncture and Massage College, Shandong University of Traditional Chinese Medicine, Jinan, Shandong, China
  5. Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, China International Neuroscience Institute (CHINA-INI), National Medical Center for Neurological Disorders, Beijing, China
  6. Institute of Literature in Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China
Journal: Frontiers in immunology, volume 17, article 1780159
Dates: received 3 January 2026; accepted 31 March 2026; published online 21 April 2026
Type: Research article · Language: English
License: CC BY
Identifiers: DOI 10.3389/fimmu.2026.1780159 · PMID 42093975 · PMCID PMC13139340 · OpenAlex W7155054269
Open access: gold, a free copy (OpenAlex)
Status: data only
Categories: genetics / omics (modality), human (organism), other condition (population)
Methods: Statistics, Smoothing, state filtering, decompositions, Preprocessing
Keywords: biochanin A, glioma, GSTP1, immunity, single-cell RNA sequencing, solid tumor, tumor microenvironment
MeSH: Brain Neoplasms*, Genistein*, Glioma*, Animals, Cell Line, Tumor, Gene Expression Regulation, Neoplastic, Glutathione S-Transferase pi, Humans, Medicine, Chinese Traditional, Prognosis, Tumor Microenvironment (* major topic)
Topic: Ferroptosis and cancer prognosis (Pulmonary and Respiratory Medicine, Medicine), according to OpenAlex
Citations: not cited yet (Europe PMC); 87 references in the paper

Abstract

Introduction: Glioma is a common primary solid brain tumor with high incidence and poor prognosis. Biochanin A (bioA), an active component of traditional Chinese medicine, has potential therapeutic effects on it, but its mechanism remains unclear. This study aimed to clarify its mechanism via a multi-omics strategy.

Methods: A multi-omics integration approach was adopted, which combined single-cell RNA sequencing, in vitro experiments, the construction of a Glutathione S-transferase P1 (GSTP1)-based prognostic model, and analyses of immune infiltration and drug sensitivity to evaluate its clinical value.

Results: C2 CENPF⁺ tumor cells were specifically expressed in recurrent gliomas and associated with the bioA pathway. GSTP1 was the key target gene of bioA; its high expression was related to poor prognosis, and its knockout could inhibit glioma progression. The GSTP1-based prognostic model had excellent predictive efficiency.

Discussion: BioA may exert anti-glioma effects by regulating GSTP1, providing theoretical support for its clinical application and a new therapeutic target for glioma.

Reproduced under the paper's license (CC BY), from the paper cited above.

Code

The paper links to its data, not to its authors' code: see the Data section.

Tracing map

A tracing map links a paper to the code its authors published: this paper has none, so it has no map.

Data

Datasets cited

Data availability statement

The original contributions presented in the study are included in the article/Supplementary Material. Further inquiries can be directed to the corresponding authors.

Reproduced under the paper's license (CC BY), from the paper cited above.

Versions

The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.

Version 1, 29 September 2026: the first record

Recorded: type, language, journal, volume, pages, dates, 10 authors, 7 keywords, 11 MeSH terms, 87 references.

Cite

This paper

Chai, D., Xi, M., Gao, L., Sun, L., Kong, D., Zhu, Y., Zhang, J., Cai, Q., Xiao, X., & Wang, C. (2026). The therapeutic effect and specific mechanism involved active Chinese medicine component biochaninA in glioma. Frontiers in immunology, 17, 1780159. https://doi.org/10.3389/fimmu.2026.1780159

BibTeX

@article{chai2026therapeutic,
author = {Chai, Dan and Xi, Mengran and Gao, Lu and Sun, Lei and Kong, Desong and Zhu, Yujie and Zhang, Jinghua and Cai, Qiang and Xiao, Xinru and Wang, Changqing},
title = {{The therapeutic effect and specific mechanism involved active Chinese medicine component biochaninA in glioma}},
journal = {Frontiers in immunology},
year = {2026},
month = apr,
volume = {17},
pages = {1780159},
publisher = {Frontiers Media SA},
issn = {1664-3224},
doi = {10.3389/fimmu.2026.1780159},
url = {https://doi.org/10.3389/fimmu.2026.1780159},
pmid = {42093975},
pmcid = {PMC13139340}
}

RIS

TY - JOUR
AU - Chai, Dan
AU - Xi, Mengran
AU - Gao, Lu
AU - Sun, Lei
AU - Kong, Desong
AU - Zhu, Yujie
AU - Zhang, Jinghua
AU - Cai, Qiang
AU - Xiao, Xinru
AU - Wang, Changqing
TI - The therapeutic effect and specific mechanism involved active Chinese medicine component biochaninA in glioma
T2 - Frontiers in immunology
J2 - Front Immunol
PY - 2026
DA - 2026/04/21
VL - 17
SP - 1780159
SN - 1664-3224
PB - Frontiers Media SA
DO - 10.3389/fimmu.2026.1780159
UR - https://doi.org/10.3389/fimmu.2026.1780159
LA - en
ER -

CSL-JSON

{
"id": "10.3389/fimmu.2026.1780159",
"type": "article-journal",
"title": "The therapeutic effect and specific mechanism involved active Chinese medicine component biochaninA in glioma",
"container-title": "Frontiers in immunology",
"author": [
{
"family": "Chai",
"given": "Dan"
},
{
"family": "Xi",
"given": "Mengran"
},
{
"family": "Gao",
"given": "Lu"
},
{
"family": "Sun",
"given": "Lei"
},
{
"family": "Kong",
"given": "Desong"
},
{
"family": "Zhu",
"given": "Yujie"
},
{
"family": "Zhang",
"given": "Jinghua"
},
{
"family": "Cai",
"given": "Qiang"
},
{
"family": "Xiao",
"given": "Xinru"
},
{
"family": "Wang",
"given": "Changqing"
}
],
"container-title-short": "Front Immunol",
"volume": "17",
"page": "1780159",
"DOI": "10.3389/fimmu.2026.1780159",
"PMID": "42093975",
"PMCID": "PMC13139340",
"ISSN": "1664-3224",
"publisher": "Frontiers Media SA",
"URL": "https://doi.org/10.3389/fimmu.2026.1780159",
"language": "en",
"issued": {
"date-parts": [
[
2026,
4,
21
]
]
}
}

Similar papers

The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.

[1] doi:10.1016/j.isci.2026.115982 [code]
Multi-omics profiling-derived signature links cellular ecosystem to glioblastoma prognosis.
Journal: iScience
In common: NCBI GEO GSE182109, genetics / omics, other condition
[2] doi:10.3389/fonc.2026.1742452
SLC10A3 drives glioblastoma progression by remodeling the immunosuppressive microenvironment and promoting M2 macrophage migration.
Journal: Frontiers in oncology
In common: NCBI GEO GSE182109, genetics / omics, other condition
[3] doi:10.32604/or.2026.079221
Single-Cell Sequencing Reveals the Heterogeneity of Glioma and Identifies IGFBP2 as A Potential Therapeutic Target.
Journal: Oncology research
In common: genetics / omics, other condition, 2 references
[4] doi:10.1080/17501911.2026.2691031
Promoter methylation-associated brain-enriched long noncoding RNAs in glioblastoma: a multi-cohort public epigenomic re-analysis.
Journal: Epigenomics
In common: genetics / omics, other condition, 2 references
[5] doi:10.1186/s13024-026-00946-0
Insulin resistance alters cortical inhibitory neurons and microglia to exacerbate Alzheimer's knock-in mouse phenotypes.
Journal: Molecular neurodegeneration
In common: genetics / omics, other condition, 2 references
[6] doi:10.1038/s41586-026-10641-1 [code]
Dual tumour-myeloid targeting of glioblastoma with GPNMB CAR-T cells.
Journal: Nature
In common: other condition, 2 references
[7] doi:10.1038/s41467-026-74058-0
IQGAP3 bridges matrix stiffness with glioma stem cell maintenance and radioresistance by stabilizing SOX2.
Journal: Nature communications
In common: other condition, 2 references
[8] doi:10.1111/jcmm.71154
Mitophagy-Oxidative Stress Molecular Subtypes Define an Immunosuppressive Ecosystem and Vulnerabilities in Glioblastoma.
Journal: Journal of cellular and molecular medicine
In common: genetics / omics, other condition, 2 references
[9] doi:10.3389/fonc.2026.1834400
BrainFusionNet: an attention-augmented deep convolutional framework with hybrid loss optimisation and test-time augmentation for multi-class brain tumour detection in magnetic resonance images.
Journal: Frontiers in oncology
In common: other condition, 2 references
[10] doi:10.1007/s12311-026-02006-1 [code]
Innovative 3D-Image Analysis of Cerebellar Vascularization Highlights Angiogenic Gene Dysregulations in a Murine Model of Apnea of Prematurity.
Journal: Cerebellum (London, England)
In common: genetics / omics, 2 references

Contribute

The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.

Sign in with ORCID to claim this paper as one of its authors, correct its record or validate its tracing map: when the paper's metadata lists your ORCID iD, you are recognized at once. Maintainers of its code: sign in with GitHub, then claim the repository on your account page.

Request its removal

To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).

Discussion, reproductions, activity

Discussion: questions and error reports about this paper and its code, from signed-in readers and its authors. It opens with sign-in.

Reproductions: reports from readers who ran the authors' code: what they reproduced, with which environment, commit and data. It opens with sign-in.

Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.